We have discovered that scattered light intensity fluctuations (SLIF) are present in isolated rat ventricular muscle even under conditions formerly considered to be quiescent. Subsequent experiments indicated that SLIF are highly dependent on calcium loading of the cell and could be reversibly terminated (1) by maintaining constant calcium concentration in the myofilament space in skinned fibers or (2) in intact fibers by caffeine. These results were interpreted to indicate that cellular myoplasmic calcium concentration oscillates in diastole, producing motion of the myofilaments, which modulates the laser beam and results in SLIF. This myofilament motion which is asynchronous within a cell, and among cells, results in a small degree of diastolc force or "tone" in the muscle. Additional experiments have demonstrated SLIF in atrial, ventricular, and conduction tissues in a range of mammalian species including man and indicate the universality of this phenomenon in excitable cardiac tissues. In collaboration with the Department of Physiology at the University of Maryland, we have directly demonstrated these Ca2+ oscillations utilizing intracellular injects of the chemiluminescent protein, aequorin. In our most recent studies we have time gated SLIF measurements in a diastolic window following stimulation in order to determine the effects of stimulation on calcium loading and to determine whether certain antiarrhythmic drugs used to treat Ca2+ dependent arrhythmias had an effect on post stimulation SLIF. We found that stimulation increases SLIF frequency in this diastolic window and that antiarrhythmias suppress this increase.